Experimental study on the deformation localisation and acoustic emission characteristics of coal in Brazilian splitting tests.

This paper presents an experimental study to assess the behaviour of coal samples under tensile loadings to better understand the failure mechanisms and the interactions with the coal characteristics. A set of Brazilian splitting tests were carried out using disk specimens obtained from Tashan Coal Mine in China. The digital speckle correlation method and acoustic emission (AE) were used to capture the deformation localisation and AE characteristics of each specimen during the loading process. The precursor characteristics of AE and the failure mechanism are discussed. It was found that the entire loading process mainly consists of compaction, elastic and post-peak dropping stage without an obvious yielding stage. Two kinds of deformation localisation were observed: central symmetry and axis symmetry. The corresponding AE evolution patterns have different phases, including gradual rise, step rise, transient rise and steady rise. During the subcritical failure stage, AE counts demonstrate a "rapidly increasing + flatten" intermittent feature. The results provide a reference for a better understanding of the damage process of the brittle coal material and its application in ground control design.

miR-19a/b-3p promotes inflammation during cerebral ischemia/reperfusion injury via SIRT1/FoxO3/SPHK1 pathway.

BACKGROUND: Stroke affects 3-4% of adults and kills numerous people each year. Recovering blood flow with minimal reperfusion-induced injury is crucial. However, the mechanisms underlying reperfusion-induced injury, particularly inflammation, are not well understood. Here, we investigated the function of miR-19a/b-3p/SIRT1/FoxO3/SPHK1 axis in ischemia/reperfusion (I/R). METHODS: MCAO (middle cerebral artery occlusion) reperfusion rat model was used as the in vivo model of I/R. Cultured neuronal cells subjected to OGD/R (oxygen glucose deprivation/reperfusion) were used as the in vitro model of I/R. MTT assay was used to assess cell viability and TUNEL staining was used to measure cell apoptosis. H&E staining was employed to examine cell morphology. qRT-PCR and western blot were performed to determine levels of miR-19a/b-3p, SIRT1, FoxO3, SPHK1, NF-κB p65, and cytokines like TNF-α, IL-6, and IL-1ß. EMSA and ChIP were performed to validate the interaction of FoxO3 with SPHK1 promoter. Dual luciferase assay and RIP were used to verify the binding of miR-19a/b-3p with SIRT1 mRNA. RESULTS: miR-19a/b-3p, FoxO3, SPHK1, NF-κB p65, and cytokines were elevated while SIRT1 was reduced in brain tissues following MCAO/reperfusion or in cells upon OGD/R. Knockdown of SPHK1 or FoxO3 suppressed I/R-induced inflammation and cell death. Furthermore, knockdown of FoxO3 reversed the effects of SIRT1 knockdown. Inhibition of the miR-19a/b-3p suppressed inflammation and this suppression was blocked by SIRT1 knockdown. FoxO3 bound SPHK1 promoter and activated its transcription. miR-19a/b-3p directly targeted SIRT1 mRNA. CONCLUSION: miR-19a/b-3p promotes inflammatory responses during I/R via targeting SIRT1/FoxO3/SPHK1 axis.

Inordinate glucose variation poststroke is associated with poor neurological improvement in patients without history of diabetes.

INTRODUCTION: Glucose variation is an important risk factor for the complications of diabetes mellitus. The plasma glucose level poststroke is in continuous fluctuation. However, whether the variation influences neurological improvement remains unknown. AIMS: This observational study aimed to investigate the association of glucose variation with neurological improvement poststroke. METHODS: We consecutively enrolled 216 ischemic stroke patients with no history of diabetes mellitus within 72 h of onset, with instant blood glucose <11.1 mmol/L at admission. The glucometabolic status was evaluated by an oral glucose tolerance test 1 day after admission and 14 days after stroke, respectively. The severity of neurological deficit was assessed with the National Institute of Health Stroke Scale (NIHSS). RESULTS: Fourteen days after stroke, 31% patients were found to have impaired glucose tolerance and 30.6% were newly diagnosed diabetes mellitus by oral glucose tolerance test. A higher level of instant blood glucose at admission or fasting plasma glucose (FPG) at 1 day correlated with a less neurological improvement. The number of patients with no <20% decrease in NIHSS was significantly decreased in patient group with higher than 30% variation of either FPG or 2-h postprandial glucose. Similar correlation between glucose variation and neurological improvement was also found in 117 patients with 2-h postprandial glucose ≥7.8 mmol/L at 1 day. CONCLUSIONS: Inordinate glucose variation correlated with less neurological improvement poststroke, giving the evidence that the fluctuation of glucose levels in stroke patients should be taken into consideration during glucose modulation.

[Association of plasma homocysteine and cystathionine beta-synthase polymorphism with cerebral thrombosis].

OBJECTIVE: To study the association of plasma homocysteine (Hcy) and polymorphism and cystathionine beta-synthase (CBS) with cerebral thrombosis. METHODS: Eighty-seven patients with first-ever acute cerebral thrombosis and 80 control subjects were examined for plasma Hcy levels using high-performance liquid chromatography-fluorescence detection and for CBS polymorphism determined by amplification refractory mutation system. RESULTS: The fasting plasma Hcy level was l5.28 micromol/L (95% CI 14.37-16.19 micromol/L) in the patient group, higher than that in the control group (11.32 micromol/L, 95% C1 10.47-12.16 micromol/L, P<0.001). Plasma Hcy levels varied with different genotypes. No difference in genotype or allele frequencies was noted between patient group and control group (P>0.05). CONCLUSION: Common mutations in CBS G919A and CBS T833C lead to hyperhomocysteinemia, which, instead of common mutations in CBS, is more directly associated with increased risk of cerebral thrombosis.

[Early diagnosis and treatment of intracranial venous thrombosis].

OBJECTIVE: To study the early diagnosis and treatment of intracranial venous thrombosis. METHOD: The etiology, clinical manifestations, presentations in cerebral CT and magnetic resonance imaging (MRI), electroencephalogram (EEG) features, and the results of cerebral spinal fluid and blood rheological examinations were analyzed in 8 cases of intracranial venous thrombosis. RESULTS: Thrombosis often arose during the puerperium and from infection, with the frequent presentations of intracranial hypertension and focal neurological defect. CT and MRI examinations were helpful in the diagnosis. CONCLUSION: For patients who present both intracranial hypertension and focal neurological defects, especially during the puerperium or with infection episodes, CT and MRI examinations should be performed to detect intracranial venous thrombosis.